Key Clinical Message : Amiodarone induced torsade de pointes is
very rare tachyarrhythmia developed during intravenous therapy for
atrial fibrillation. Careful monitoring of the QT interval can prevent
development of this life-threatening arrhythmia.
Introduction: Amiodarone is a class III antiarrhythmic agent
with a low frequency of pro-arrhythmic effect and an incidence of
torsade de pointes (TdP) of <1.0% (1-3). Intravenous (IV)
amiodarone is useful for the treatment of atrial fibrillation and
ventricular tachyarrhythmias (4). We presented the rare case of a woman
with rapid atrial fibrillation (AF) who developed TdP on day 3 of
intravenous amiodarone therapy.
Case Report: A 71 year-old woman with a history of diabetes
mellitus and hypertension treated with metformin and bisoprolol 2.5 mg,
admitted with palpitations and dyspnea for two days. An examination
revealed wheezing on the base of the lungs and rapid AF on ECG with QT
interval of 326 msec, QTc 405 msec (Fig.1). Transoesophageal
echocardiogram excluded left atrial thrombus and showed preserved left
ventricular function. Electrical cardioversion to NSR was done and
infusion of amiodarone 1 mg/min for 6 hours, then 0.5 mg/min for 18
hours started after 150 mg bolus. Soon atrial fibrillation developed
again. For treatment after the first 24h, the maintenance infusion of
amiodarone 0.5 mg/min was continued. Electrolytes were in the normal
ranges. On the third day of hospitalization, an electrical cardioversion
to NSR was done again after an additional 150 mg bolus of amiodarone. In
the evening recurrent episodes of TdP were developed and need to
electrical cardioversion (Fig.2). ECG revealed QT prolongation (511
msec, QTc 531 msec). The amiodarone was discontinued. An insertion of
temporal pacemaker for 2 days was required to suppress this
life-threatening arrhythmia (Fig.3). The QT interval gradually decreased
to its baseline value after cessation of the intravenous amiodarone.
Discussion: Although therapy with amiodarone is generally
considered safe, torsades de pointes can be developed after intravenous
use of the drug (5-6). Amiodarone act by blocking different ion channels
involving in the action potential with a dominant effect on potassium
channels and therefore can prolong QT interval. The drug also causes
bradycardia by suppressing the sinus node and atrio-ventricular
conduction. Intravenous amiodarone significant slow intraventricular
conduction and does not prevent the inducibility of ventricular
tachycardia (7-8). In addition to route, dose and rate administration,
other predisposing factors to amiodarone induced TdP may be electrolyte
disturbances and bradycardia due to concomitant drugs such as beta
blockers and/or digoxin (9). The arrhythmia is more common in women
(10).
Our patient was a woman treated with a low dose of beta-blocker on the
day of start amiodarone infusion. It may be preferable to avoid
initiation of IV amiodarone with beta-blocker. The patient admitted with
rapid atrial fibrillation and pulmonary congestion and we need to do
cardioversion and start antiarrhythmic drug. Soon after electrical
cardioversion to normal sinus rhythm and intravenous amiodarone therapy,
her heart rhythm again returned to rapid atrial fibrillation. We
continued to treat our patient with IV amiodarone. During this time she
was on ECG monitoring, but without regular measurement of QT interval.
On the third day we gave additional bolus of amiodarone 150 mg and after
that did cardioversion. In this evening amiodarone induced TdP was
developed. Significant QT prolongation was revealed on ECG.
Usually amiodarone induced TdP occurs within 24h after initiation of the
therapy. In our case it occurred on day 3 of the maintenance infusion of
amiodarone. Perhaps we didn’t have to give an additional bolus of
amiodarone before the second cardioversion of atrial fibrillation.
Conclusions: C areful monitoring of the QT interval during
intravenous amiodarone therapy can prevent development of
amiodarone-induced TdP.